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Background <p>Pulmonary infections caused by microorganisms in lung cancer patients contribute to disease progression and treatment challenges. This systematic review aims to explore the clinical and pathophysiological characteristics of microbial pulmonary infections in lung cancer.</p> Methods <p>A systematic literature search was conducted across Embase, PubMed/MEDLINE, Scopus, and Web of Science, covering studies published between January 1, 2015 and February 1, 2025, without restrictions on population or language. We included original studies reporting findings in human, animal, cell, or in silico models that examined non-viral microbial pulmonary infections in the context of lung cancer, with a focus on pathogen profiles, antimicrobial resistance, and associated molecular mechanisms. Evidence synthesis was narrative.</p> Results <p>A total of 8,879 records were identified, with 37 studies included comprising 14 human, 14 in vitro, 8 in vivo and one in silico studies. Of the 14 human studies, 8 studies reported microbial strain prevalence in 2,598 lung cancer patients. The most common pathogens included <i>Klebsiella pneumoniae</i> (21.1%), <i>Pseudomonas aeruginosa</i> (17.0%), <i>Staphylococcus</i> spp. (16.1%), <i>Streptococcus</i> spp. (14.1%), <i>Candida</i> spp. (12.4%), <i>Haemophilus influenzae</i> (7.9%), <i>Enterobacter</i> spp. (7.7%), and <i>Aspergillus</i> spp. (3.1%). Antibiotic sensitivity varied, with <i>K. pneumoniae</i> showing complete sensitivity to tigecycline and <i>S. pneumoniae</i> exhibiting low clindamycin sensitivity (~6%). Mechanistic studies identified key molecular pathways, including PD-1/PD-L1, NF-κB, and TLR4/MyD88, linking microbial pulmonary infections to lung cancer progression.</p> Conclusion <p>Pulmonary infections play a significant role in lung cancer pathogenesis, particularly infections caused by <i>K. pneumoniae</i> and <i>P. aeruginosa</i>, potentially by triggering immune evasion and inflammatory signaling pathways.</p> Graphical Abstract <p></p>

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Pathogenic mechanisms and resistance profiles of microbial pulmonary infections in lung cancer: a systematic review

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月5日

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  • Milad Sheervalilou,
  • Mostafa Ghanei,
  • Masoud Arabfard

摘要

Background

Pulmonary infections caused by microorganisms in lung cancer patients contribute to disease progression and treatment challenges. This systematic review aims to explore the clinical and pathophysiological characteristics of microbial pulmonary infections in lung cancer.

Methods

A systematic literature search was conducted across Embase, PubMed/MEDLINE, Scopus, and Web of Science, covering studies published between January 1, 2015 and February 1, 2025, without restrictions on population or language. We included original studies reporting findings in human, animal, cell, or in silico models that examined non-viral microbial pulmonary infections in the context of lung cancer, with a focus on pathogen profiles, antimicrobial resistance, and associated molecular mechanisms. Evidence synthesis was narrative.

Results

A total of 8,879 records were identified, with 37 studies included comprising 14 human, 14 in vitro, 8 in vivo and one in silico studies. Of the 14 human studies, 8 studies reported microbial strain prevalence in 2,598 lung cancer patients. The most common pathogens included Klebsiella pneumoniae (21.1%), Pseudomonas aeruginosa (17.0%), Staphylococcus spp. (16.1%), Streptococcus spp. (14.1%), Candida spp. (12.4%), Haemophilus influenzae (7.9%), Enterobacter spp. (7.7%), and Aspergillus spp. (3.1%). Antibiotic sensitivity varied, with K. pneumoniae showing complete sensitivity to tigecycline and S. pneumoniae exhibiting low clindamycin sensitivity (~6%). Mechanistic studies identified key molecular pathways, including PD-1/PD-L1, NF-κB, and TLR4/MyD88, linking microbial pulmonary infections to lung cancer progression.

Conclusion

Pulmonary infections play a significant role in lung cancer pathogenesis, particularly infections caused by K. pneumoniae and P. aeruginosa, potentially by triggering immune evasion and inflammatory signaling pathways.

Graphical Abstract